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The aim of this study was to demonstrate the macrovascular disease in streptozotocin-induced diabetic rats and assess any possible differences between the histopatholological changes of the coronaries and cerebral arteries. Hearts and brains were obtained after 4 weeks (short-term experimental diabetes, 10 rats) and 12 weeks (long-term experimental diabetes, 10 rats) of streptozotocin injection. Sham injected, control rats were studied in parallel. Muscular-type arteries of 0.10-0.15 mm were examined and semiquantitatively classified either as normal, or slightly, or moderately, or severely thickened by light microscopy: While the arterial wall appeared normal in all sham-injected rats, a varying degree of hyperplasia of the muscular layer and deposition of fibrinoid material resulting in arterial stenosis was prominent in streptozotocin-injected rats. In the group of short-term diabetes there was a slight thickening of the cerebral arteries in the majority of the rats (8/10 rats), while thickening of the coronaries was moderate (9/10 rats). Further progression of arterial wall thickening in both cerebral and coronary arteries was observed in the long-term diabetic group. The mean severity of lesions was significantly higher in the coronaries than in cerebral arteries, both in the short-term (p < 0.0005) and long-term diabetes (p < 0.02). Moreover, by paired statistics within individual animals, we confirmed that wall thickening was significantly more severe in coronaries than cerebral arteries in both groups. These findings suggest an accelerated progress of macrovascular disease in the heart as compared to the brain in the streptozotocin-induced diabetic rat. Although histopathological changes in humans do not always mirror clinical severity, the differences in the macrovascular disease between heart and brain in experimental diabetes may be relevant to the higher relative risk of myocardial infarction compared to stroke for people with diabetes, as compared to people without diabetes.

Background and aim: Postprandial glycaemia and lipaemia are known risk factors for atherosclerosis in type 2 diabetes. Coagulation activation in the postprandial. state also contributes to acceleration of atherosclerosis. Nateglinide is effective in reducing postprandial glycaemia. Its effect on glycaemia may also be beneficial in postprandial lipaemia and coagulation. The aim of this study was to examine the potential effect of a single dose of nateglinide on postprandial triglyceridaemia, coagulation, and fibrinolysis in patients with type 2 diabetes. Methods and results: Ten subjects with type 2 diabetes, treated with diet alone were recruited in a crossover randomized study. In the morning, after a 12- to 14-h fast, each subject received a standard mixed meat (total energy 783 kcal), preceded by one tablet of 120 mg nateglinide or placebo. Venous blood samples were drawn prior to meat consumption and 6 h afterwards for the measurement of plasma glucose, insulin, and C-peptide, lipids, coagulation, and fibrinolysis factors. As expected, there was a significant reduction in postprandial glycaemia after nateglinide administration compared to placebo (P &LT; 0.001). Plasma insulin levels were significantly higher after nateglinide than after placebo (P = 0.002). Nateglinide administration resulted in a lower overall postprandial reduction of tissue-plasminogen activator than placebo (-2.9 &PLUSMN; 1.3 vs. -8.3 &PLUSMN; 3.7 ng/ml h, P = 0.003). In addition, a significant reduction of postprandial plasminogen activator inhibitor-1 was observed in comparison with the baseline values after nateglinide (P = 0.001), although the overall response was not significantly different after nateglinide and placebo (P = 0.31). Plasma concentrations of C-peptide, lipids and the remaining coagulation parameters studied were not different between nateglinide and placebo. Conclusions: Acute nateglinide administration improves postprandial glycaemia and fibrinolytic activity in patients with type 2 diabetes. This combined effect, if confirmed by a long-treatment study, might reduce cardiovascular risk in type 2 diabetes. &COPY; 2005 Published by Elsevier Ltd. Nutrition Metabolism and Cardiovascular Diseases

Diabetic foot ulceration is currently a serious medical problem and has, therefore, attracted much research attention during the last two decades. Previous foot ulceration, diabetic neuropathy, limited joint mobility, high plantar pressures, microangiopathy, macroangiopathy and diabetic nephropathy have already been identified as risk factors for future foot ulceration. Neuropathy has clearly been shown to be an essential permissive factor in the development of ulceration in the non-ischaemic foot. Moreover, the pathogenetic role of high plantar pressures is crucial in the presence of established clinical neuropathy. Nowadays, our therapeutic efforts clearly aim to prevent than treat foot ulcers. This demands specialist and team work in the setting up of a diabetic foot clinic in an attempt to identify and educate the diabetic patients at risk and, where possible to use suitable plantar pressure-reducing systems (footwear, hosiery etc.). Then only would it be reasonable to postulate that a significant reduction in amputations of diabetic aetiology could be achieved in the near future.

Summary OBJECTIVE The few published prospective studies suggest a strong association of colonic tumours with acromegaly, but include small numbers of patients. In addition, the upper gastrointestinal tract of these patients has never been prospectively studied. The aim of the present study was to investigate the incidence of gastric and colonic tumours in a large cohort of acromegalic patients. DESIGN Acromegalic patients consecutively admitted to an Endocrinology Department for diagnosls and follow-up, were submitted to gastroscopy and colonoscopy, to identify those harbouring gastrointestinal tumours. PATIENTS Over a 5-year period, 54 out of 61 patients (78% with active disease) received colonoscopy and 42 out of 61 gastroscopy. No patient had a past history of gastrointestinal malignancy. MEASUREMENTS All polypoid lesion8 found at colonoscopy and gastroscopy were separately recorded and biopsled. RESULTS No case of gastrointestinal cancer or gastric polyp was discovered. Nineteen patients (35%) had 1-8 colonic polyps, including 5 (9·3%) with adenomas. When compared to patients with a normal colon, those with polyps were significantly older (44·±14· vs 52· f 10·9 years, P= 0·47), but the duration of acromegaly (10·±8· vs 10·±7· years, P= 0·9) and the number of patients with active disease were similar in both groups. CONCLUSIONS Acromegalic patients do not have an increased incidence of gastric tumours. The observed significant variation in the prevalence of colonic adenomas (9-35%, P= 0·03) and cancer (0-15%, P= 0·017), between our patients and those of the published prospective studies with similar demographic characteristics, suggest that environmental and hereditary factors may be more important than the presence of acromegaly.

The magnitude of complex carbohydrate malabsorption in exocrine pancreatic insufficiency has not been well quantified in the past. The quantity of carbohydrate malabsorbed after a rice starch (100 g) meal in 20 patients with chronic pancreatitis (n = 10) or pancreatic cancer (n = 10) was therefore estimated. Patients had a three day stool fat collection (80 g/24 hour fat intake), a lactulose (20 g), and a rice flour (100 g) breath hydrogen test. Normal controls (n = 29) had a postprandial H2 increase < or = 14 ppm and malabsorbed (mean (SEM)) 1.12 (0.44) (range 0-11.10) g of the 100 g of carbohydrate ingested. Patients malabsorbed significantly more carbohydrate (11.36 (2.23) (range 8.90-32.60) g, F1.47 = 29.92, p < 0.001). The number of patients with fat (> 7 g, n = 8) or carbohydrate (increase in H2 > or = 20 ppm, n = 10) malabsorption was not different (chi 2 = 0.10, p = 0.75). There was a significant correlation between faecal fat and amount of malabsorbed carbohydrate (r = 0.60, F1.17 = 9.70, p = 0.006) and faecal fat and stool wet weight (r = 0.57, F1.18 = 8.67, p < 0.009), but not between stool wet weight and amount of malabsorbed carbohydrate (r = 0.28, F1.17 = 1.45, p = 0.25). Although patients with exocrine pancreatic insufficiency malabsorb 10%-30% of the ingested complex carbohydrate, the main determinant of stool wet weight could be faecal fat.

The alpha-glucosidase inhibitors acarbose and miglitol have been successfully used to control postprandial hyperglycaemia in diabetics. They probably work by slowing carbohydrate digestion and absorption, but their effect on mouth to caecum transit time has not been studied. The effect acarbose (100 mg), miglitol (100 mg), and placebo on mouth to caecum transit time (380 kcal breakfast with 20 g of lactulose) was investigated in 18 normal volunteers using breath hydrogen analysis. Both miglitol and acarbose significantly increased breath hydrogen excretion (F2,34 = 6.31, p = 0.005) and shortened the mouth to caecum transit time (F2,34 = 3.49, p = 0.04) after breakfast compared with placebo. There was a significant negative correlation between breath hydrogen excretion and mouth to caecum transit time suggesting that with shorter transit times significantly more carbohydrates were spilled into the colon. These results indicate that alpha-glucosidase inhibitors accelerate mouth to caecum transit time by inducing carbohydrate malabsorption.

Organ transplantation depends on a display of public confidence. Health authorities have the duty to protect public confidence against any action that would put in doubt the quality of the health services offered and/or the ethical issues connected with the health services. On the other hand, there has been a period of access to the practice of “transplantation on the free market”, something which creeping its way in to several countries and which will hopefully come to an end shortly. Our aim is to present another aspect of commercialism, more complicated than usual, and in which conflicting evidence has been presented at different periods; this aspect will also be ending soon.

Our purpose was to describe the first in our country and fourth worldwide simultaneous liver and renal grafting for polycystic disease.